Hockenberry: Wongs Nursing Care of Infants and Children, 10th Edition

Chapter 33: The Child with Endocrine Dysfunction

Key Points - Print

The endocrine system has three components: the cell, which sends a chemical message via
a hormone; target cells, which receive the message; and the environment through which the
chemical is transported from the site of synthesis to the sites of cellular action.
Deficiencies of the anterior pituitary hormones may be due to organic defects or have an
idiopathic etiology and may occur as a single hormonal problem or in combination with
other hormonal deficiencies. Pituitary dysfunction is manifested primarily by growth
disturbance.
Hypopituitarism is diminished or deficient secretion of pituitary hormones. The
consequences of the condition depend on the degree of dysfunction. It often leads
to:
Gonadotropin deficiency with absence or regression of secondary sexual
characteristics
Growth hormone (GH) deficiency, in which children display retarded somatic
growth
Thyroid-stimulating hormone deficiency, which produces hypothyroidism
Corticotropin deficiency, which results in manifestations of adrenal hypofunction
The principal disorder of posterior pituitary hypofunction is diabetes insipidus (DI).
Also known as neurogenic DI, central diabetes insipidus results from the
undersecretion of antidiuretic hormone (ADH), also known as vasopressin.
Oversecretion of the posterior pituitary antidiuretic hormone (ADH) causes the disorder
known as syndrome of inappropriate antidiuretic hormone (SIADH).
Disorders of thyroid function include hypothyroidism, autoimmune thyroiditis, goiter,
and hyperthyroidism.
Growth cessation or retardation in a child whose growth has previously been normal should
alert the observer to the possibility of hypothyroidism. Children with hypopituitarism
generally grow normally during the first year and then follow a slowed growth curve that is
below the third percentile. In children with a partial GH deficiency, the growth retardation is
less marked than in children with complete GH deficiency. Height may be retarded more
than weight because, with good nutrition, these children can become overweight or even
obese.
A complete diagnostic evaluation should include a family history, a history of the childs
growth patterns and previous health status, physical examination, psychosocial
evaluation, radiographic surveys, and endocrine studies.
Lymphocytic thyroiditis (also known as Hashimoto disease or juvenile autoimmune
thyroiditis) is the most common cause of thyroid disease in children. The enlarged thyroid
gland is usually detected by the practitioner during a routine examination, although it may
be noted by parents when the youngster swallows. In most children, the entire gland is
enlarged symmetrically (although it may be asymmetric) and is firm, freely movable, and
nontender.
Therapy for hyperthyroidism is directed at retarding the rate of hormone secretion and
may include drug therapy, thyroidectomy, or radioiodine therapy.
Copyright 2015, 2011, 2007, 2003, 1999 by Mosby, Inc., an imprint of Elsevier Inc. All rights reserved.
Key Points - Print 33-2

Classic forms of hypoparathyroidism in childhood are idiopathic (involving a deficient

production of parathyroid hormone) and pseudohypoparathyroidism (involving
increased parathyroid hormone production with end-organ unresponsiveness to the
hormone).
The adrenal cortex secretes three important groups of hormones:
glucocorticoids, mineralocorticoids, and sex steroids.
Disorders of adrenal function include acute adrenocortical insufficiency, chronic
adrenocortical insufficiency, Cushing syndrome, congenital adrenal hyperplasia,
and hyperaldosteronism.
Cushing syndrome is a characteristic group of manifestations caused by excessive
circulating free cortisol. The five categories of Cushing syndrome are pituitary, adrenal,
ectopic, iatrogenic, and food dependent. Because the actions of cortisol are widespread,
clinical manifestations are equally profound and diverse. The physiologic disturbances,
such as hyperglycemia, susceptibility to infection, hypertension, and hypokalemia, may
have life-threatening consequences unless recognized early and treated successfully.
Congenital adrenal hyperplasia is a family of disorders caused by decreased
enzyme activity required for cortisol production in the adrenal cortex. Management
includes assignment of a sex according to genotype; administration of cortisone; and,
possibly, reconstructive surgery.
Diabetes mellitus is a chronic disorder of metabolism characterized by a partial or complete
deficiency of the hormone insulin. Type 1 diabetes is characterized by destruction of the
pancreatic beta cells, which produce insulin. This usually leads to absolute insulin
deficiency. Type 2 diabetes usually arises because of insulin resistance, in which the body
fails to use insulin properly, combined with relative (rather than absolute) insulin deficiency.
People with type 2 diabetes can range from predominantly insulin resistant with relative
insulin deficiency to predominantly deficient in insulin secretion with some insulin
resistance.
Three groups of children who should be evaluated for diabetes are (1) children who have
glycosuria, polyuria, and a history of weight loss or failure to gain despite a voracious
appetite; (2) those with transient or persistent glycosuria; and (3) those who display
manifestations of metabolic acidosis, with or without stupor or coma. Diabetes should be
suspected in children with a strong family history of diabetes, especially if another child
in the family has the disease.
Diabetes is a great imitator; influenza, gastroenteritis, and appendicitis are the conditions
most often diagnosed when it turns out that the disease is really diabetes. The sequence of
chemical events results in hyperglycemia and acidosis, which produce weight loss and the
three polys of diabetespolyphagia, polydipsia, and polyuriathe cardinal symptoms
of the disease.
Management of type 1 diabetes mellitus focuses on insulin replacement, diet, and exercise.
Management requires a multidisciplinary approach involving the family; the child (when
appropriate); and professionals, including a pediatric endocrinologist, diabetes nurse
educator, nutritionist, and exercise physiologist.
Insulin replacement is the cornerstone of management of type 1 diabetes. Insulin dosage is
tailored to each child based on home blood glucose monitoring. The goal of insulin therapy
is maintaining near-normal blood glucose values while avoiding too frequent episodes of
hypoglycemia.

Copyright 2015, 2011, 2007, 2003, 1999 by Mosby, Inc., an imprint of Elsevier Inc. All rights reserved.
Key Points - Print 33-3

Diabetes management involves a constant state of assessment. Daily monitoring of blood

glucose levels; periodic urinalysis for ketones; and observation for signs of hypoglycemia,
hyperglycemia, or other complications are part of the daily life of children with diabetes
and their families.
Family education includes explanation of diabetes, meal planning, administering insulin
injections, monitoring general hygienic practices, promoting exercise, record keeping,
and observing for complications.
Diabetic ketoacidosis, the most complete state of insulin deficiency, is a life-threatening
situation. Management consists of rapid assessment, adequate insulin to reduce the elevated
blood glucose level, fluids to overcome dehydration, and electrolyte replacement
(especially potassium).

Copyright 2015, 2011, 2007, 2003, 1999 by Mosby, Inc., an imprint of Elsevier Inc. All rights reserved.